Unit 4a Flashcards
Peptidoglycan layer
rigid mesh, surrounds cytoplasmic membrane
Peptidoglycan → allows for maintenance of shape and resistance of osmotic pressure
Unique and required bacterial structure
Great target for many antibiotics
Recognized by host innate immune system
Structure of peptidoglycan layer
Polymer of repeating units of 2 hexose sugars, crosslinked
N-acetylglucosamine (GlcNAc)
N-acetylmuramic acid (MurNAc): linked to tetrapeptide chains with AA unique to bacterial cell walls
Capsules
gelatinous outer surface layer, coats surface of bacterial cells
Consist of complex polysaccharides
Function: Enhance virulence, resist phagocytosis
Antigenic (used in vaccines)
-Protein-capsular polysaccharide CONJUGATE vaccine may be required to vaccinate young children
Glycocalyx
form microbial biofilms (communities of bacteria)
“Slime layer” connects/embeds bacteria together/to surfaces
Protects cells from phagocytosis, host defenses (complement, antibody, defensins), limits access of abx to cells embedded in “slime layer”
Flagella
Originate in cytoplasmic membrane
Function in motility, bacterial chemotaxis
Peritrichous = flagella distributed over their surface Polar = one/many flagella at one end
Move in a rotation: Run and Tumble based on direction of rotation
Antigenic (H antigens) - used in vaccines
Pili
long slender, proteinaceous antigenic, hair-like structure on surface of bacteria
Role in adherence to surfaces/tissues
Antibody can block adherence/confer resistance to infection
Sex pili → role in bacterial conjugation
Bacterial Secretion Systems
deliver proteins from cytoplasm of bacteria directly to target cell → alter cell function (alter actin cytoskeleton, host signaling, transcription)
Bacterial cytoplasmic membrane
- physiological barrier between inside/outside of bacterial cell
- Lipid bilayer (phospholipids, proteins (60-70%), NO sterols)
-Selective permeability
Only permeable to uncharged, hydrophobic molecules, smaller than glycerol
Contains electron transport system → generate proton motive force during respiration
Bacterial cytoplasm
aqueous solution, proteins + metabolites
-contains DNA (no nuclear membrane)
Bacterial ribosomes
70S, mRNA can be polycistronic
Bacterial nucleoid
DNA of bacteria located in this distinct region
DNA tightly packed, supercoiled
No nuclear membrane → transcription/translation coupled
Bacterial chromosome
single ds-circular DNA
Bacterial plasmid (4)
extrachromosomal, self-replicating, DNA molecules
Smaller than chromosomes
Not essential for viability
R Factors: genes that carry resistance to antibiotics
Bacteriophages
viruses that infect bacteria
Can integrate into bacterial chromosomes and replicate as part of the chromosome
Gram+ bacteria
Thick, extensively cross-linked peptidoglycan layer, also contains:
- teichoic acids
- Lipoteichoic acids
Techoic Acids
repeating polyglycerol-P or polyribitol-P backbone covalently attached to peptidoglycan layer
-embedded in peptidoglycan layer of gram + bacteria
Lipoteichoic acids
attached to underlying cytoplasmic membrane - anchors cell wall to membrane
present in gram+ bacteria
Function of teichoic acids (3)
1) Ion homeostasis
2) Adherence and colonization
3) Interacts with innate immune system through TLR for bacterial recognition and inflammation
Gram + stains ______, while gram - stains _______
purple
red
Bacterial endospores
Produced by some G+ bacteria (Clostridium, Bacillus)
Dormant (non-growing, non-metabolising) - resting stage to endure tough times - when environment improves it will grow
Highly resistant to environmental stresses, high temp, disinfectants, desiccation, oxygen
Gram- bacteria
Thin, sparsely cross-linked peptidoglycan layer with other major components on exterior of peptidoglycan
-Second outer membrane
What is contained in second outer membrane of gram-neg bacteria? (4)
asymmetric lipid bilayer
1) Lipopoilysaccharide
2) Lipoproteins
3) proins
4) phospholipids
Lipopolysaccharide (LPS) made up of ______, ______, and ______ located exclusively on the _______ of the second outer membrane.
LPS can be recognized by _________
Lipid A (endotoxin) Core polysaccharide O side chain oligosaccharides (somatic antigens, O antigen)
outer leaflet
innate immune system –> inflammation and endotoxic shock
Bacterial growth
Growth via binary fission → two cells of equal size
All bacteria are thus the same “age”
4 phases of bacterial growth
1) Lag phase
2) Exponential phase
3) Stationary phase
4) Death phase
Lag phase
period of physiologic adjustment (inoculum)
Establish proper intracellular environment for optimal growth
Exponential phase
rate of cell division maximal for available nutritional conditions
Stationary phase
essential nutrients are consumed, toxic products of metabolism accumulate
Cell growth slows or ceases
Slow growing cells can be resistant to abx
Where bacteria spend most of their time in nature
Death phase
number of viable bacteria decrease over time
Heterotrophic vs. autotrophic bacteria
Heterotrophic bacteria: require organic carbon source
Autotrophic: obtain carbon exclusively from CO2
Fastidious bacteria
require, in addition to sources of carbon/energy, a number of essential growth factors
Obligate intracellular bacteria
growth within eukaryotic cells, cannot be cultivated on artificial media
Aerobic bacteria
require oxygen for growth
Produce ROS, and thus must produce catalase, superoxide dismutase, etc. to protect themselves against ROS
Anaerobic bacteria
do not require oxygen for growth
Indifferent bacteria
ferment in presence or absence of O2
Facultative bacteria
respire with O2, ferment in absence of O2
Sporulation
response to adverse nutritional condition
Spores
specialized cells produced by certain bacteria when nutritional supply is limited
Adapted for prolonged survival under adverse conditions
Can convert back to vegetative cells via germination
______ + _______ = “Energy Currency”
ATP + electrochemical gradient
Fermentation
catabolic, organic compounds are e- donors and acceptors
No net oxidation of substrates
Anaerobic, facultative/indifferent bacteria that grow under anaerobic conditions must get energy via fermentation of organic substrates
CANNOT do respiration
Respiration
generate ATP via e- transport, use O2 as final e- acceptor
Anaerobic respiration → use inorganic substrates as e- acceptor
Mechanisms of genetic variation (3)
1) Spontaneous Mutation
2) Recombination
3) Acquisition of new DNA segments
Spontaneous mutation
spontaneous single base change, deletion, insertion
Selective pressure for preferential growth of preexisting mutant within a population
→ resistance to antimicrobials, DOES NOT HAPPEN BERY OFTEN
Recombination
Site-specific or homologous recombination within a particular organism
OR genetic exchange/recombination between closely related organisms
→ new strains, new properties
Acquisition of new DNA segments
acquire new genes by LATERAL TRANSFER from other bacteria, or unrelated species
→ Alters virulence potential, survival characteristics, or antimicrobial resistance
Transposable elements
segment of DNA contained in bacteria/phage chromosome/plasmid that is enzymatically moved from one DNA location to another
(can make it mobile if it goes to a plasmid!)
How can you acquire new DNA segments? (4)
1) Transposable elements
2) Bacteriophage conversion
3) Acquisition of plasmids
4) Acquisition of pathogenicity islands
Conjugative plasmids
self-transmissible, mediate their own transfer between cells
Non-conjugative plasmids
mobilizable - can be passively transferred during conjugation
Can still be transferred by transformation or transduction
Bacterial plasmids can be transferred by _________ in gram+ bacteria
generalized transduction
Pathogenicity Islands
Insertions of one or more genes when comparing the genomes of two isolates of same species
-Encode genes that influence pathogenicity of strain
-Often appear as if acquired from an unrelated organism
(Genetic characteristics of bacterial viruses)
-Acquisition/loss important for evolution of pathogen
Transformation
Exchange of naked DNA of naked plasmid DNA (released from lysing cells)
DNA uptake into bacterial chromosome occurs only at certain points in growth cycle - specialized proteins needed to mediate uptake
Transduction
Gene transfer mediated by bacteriophage
Bacteriophage transfers segments of plasmid or chromosomal DNA from one cell to another
Conjugation
Genetic transfer dependent upon physical contact between donor and recipient cells - mediated by bacterial plasmids
Mechanisms of conjugation:
1) Cells come in contact, conjugation initiated (sex pilus bridges F+ and F- cell)
2) ss nick on oriT and binding of protein at 5’ end (in F+ cell) → initiate rolling circle replication
3) ss DNA transferred to F- cell via bridge and complementary strand synthesized
4) Cells separate at end of transfer
Conjugative transposons
DNA element that can excise themselves to form a covalently closed circular intermediate.
-circular intermediate can either reintegrate in the same cell (intracellular transposition) or transfer by conjugation to a recipient and integrate into the recipient’s genome (intercellular transposition)
Can encode abx resistance (esp Tetracycline)
Lytic state
Adhere to bacteria, inject DNA into bacteria
Progeny virus assembly/multiplication in cell and host cell lysis
Lysogenic state:
host cell remains viable, infecting phage DNA maintained by host cell in noninfectious state = prophage
Viral DNA injected, integrates into host chromosome → replicated as part of host chromosome (keep lytic stuff silent)
Maintained by prophage-encoded repressor protein that inhibits lytic development (can transform to lytic state)
Can convert phenotype of bacterial cell by formation of a lysogen
Prophage
phage DNA passively replicated as part of bacterial chromosome
Lysogenic Conversion
Temperate bacteriophages encode gene only expressed during lysogenic state → new phenotype in lysogenic host
Genes controlling the new phenotypic trait found ONLY as a component of the phage genome (not normal constituent of bacterial genome)
Generalized transduction
Any segment of donor cell genome may be passed into another cell
Sometimes get bacterial chromosomal DNA in virus capsule instead of viral DNA as an error during phage assembly
→ Integrate piece of bacterial DNA into another bacteria cell
Staphylococcus aureus is ______, _______ and ______ positive
catalase, coagulase, and gram
Staph. aureus abx resistance (3)
ABX resistance a serious concern
1) Penicillin-R
2) Methicillin-R (MRSA)
3) Vancomycin-R (emerging)
Manifestations of disease in staph aureus is…
STRAIN DEPENDENT
3 common types of diseases with staph aureus
- Cutaneous infection (localized focal abscess, can still spread)
- Toxinogenic infections (SSSS, TSS, food poisoning)
- Pneumonia (immunosup. with ~50% mortality)
staph aureus has ______, _______, ________ and _______ associated with its cutaneous infections
1) fibrin capsule
2) coagulase
3) alpha-toxin
4) foreign bodies
Coagulase and fibrin capsule of staph aureus act to…
wall off bacteria
alpha toxin of staph aureus acts to…
Pore forming, damage tissue, interfere with phagocytosis/killing
Toxinogenic Diseases of staph aureus (3)
- Staph Scalded Skin Syndrome (exfoliatins –epidermis falls off)
- Toxic Shock Syndrome (TSS) – Local infection, syst. toxic production of superantigen (T cell activation regardless of antigenic specificity)
- Food Poisoning from super-antigen contaminated food
Where is staph aureus naturally located in the body
Anterior nares, Perineum,
Normal flora - may be source of infection
30% of people are asymptomatic carriers of staph aureus
Staphylococcus epidermidis is ______ positive but ______ negaive
gram
coagulase
abx resistance and difficulties with treating staph epidermidis
Makes BIOFILMS on devices hard to treat
-often device must be removed
Abx resistance:
1) Methicillin-R
Typical staph epidermidis infections
Localized infections associated with foreign bodies (catheters, shunts, artificial/ damaged heart valves, hip prostheses)
Staph epidermidis generates ________ which makes it hard to treat
Glycocalyx (gooey ploysac.) producers (allow organisms to adhere tenaciously to various implanted devices and grow in biofilm on device surface)
Infection with staph epidermidis
Normal skin flora
-fairly non-pathogenic, but may be associated with localized infections
Nosocomial infections
Normal flora enters on foreign body
Microbial toxins
macromolecular products of microbes which cause harm to susceptible animals by altering cellular structure or function
Can cause major manifestations of specific diseases
Can contribute to pathogenesis without causing unique signs or symptoms
Toxin-mediated diseases cause significant morbidity and mortality
Toxins that facilitate spread of microbes through tissues act by…
Examples
breaking down ECM, degrading debris
EX) hyaluronidase, collagenase, elastase, phospholipase, streptokinase, deoxyribonuclease produced/secreted by bacteria
Toxins that damage cellular membranes include ______ and ______ and act by….
hemolysins, cytolysins
Can kill target cell, form pore in membrane or degrade membrane → lyse cells
Hemolysins
made by ______ and _______
mechanism of action
(lyse RBCs) - many varieties
EX) Staph aureus, strep pneumoniae
Insert into membrane and form pore = pore forming toxins
Cytolysins
lyse RBCs and other cells too
Superantigens
most potent T cell activators, aberrant activation of T cells
Bind MHC class II on APCs and to specific V chains on T cells (at site different from antigen-binding site) → activate LARGE number of T cells
Stimulate excessive production of cytokines
______ and ______ make 19 different types of superantigens and can cause diseases such as _______, _______, and _______
Staph aureus (TSST) Strep pyogenes (pyrogenic exotoxins)
Toxic Shock Syndrome, food poisoning, necrotising fasciitis
________, ________, _______, _______ and ________ inhibits protein synthesis irreversibly
Diptheria toxin Pseudomonas aeruginosa Shiga toxins Ecoli toxin Ricin
Diptheria toxin
- Inhibits protein synthesis by modifying EF-2 in euk cells
- Toxin made locally and disseminates throughout whole body
- Specific receptors on target organisms - doesn’t affect cells that lack the specific receptor
1 molecule of diphtheria can kill 1 eukaryotic cell
If you have antitoxin you are protected against diphtheria → need immunization + boosters
Pseudomonas aeruginosa toxin
produces toxin with same mechanism as diptheria (EF-2 modifiation)
–> BUT still require different toxoid immunization
Targets different organs than diphtheria (different receptor targets)
Shiga toxins, Ecoli toxin, and Ricin
Act on ribosomal subunit to stop protein synthesis
-RNA N-glycosidases that remove residue from 60S subunit –> inactivate ribosomes
All have different effects based on receptors they target
Vibrio Cholerae toxin
- cell signal pathway modification
- increases cAMP –> active Cl- secretion –> secretory diarrhea and massive water loss
-targets small intestine
Pertussis toxin
Modify intracellular signaling pathways
Increases Adenyl cyclase activity-> increase cAMP
Anthrax edema factor (EF) and Anthrax lethal factor (LF)
Toxins that modify intracellular signaling pathways
Edema factor → increase AC activity –> increase cAMP –> water influx
Lethal factor → breaks down signaling proteins (kinases)
Toxins that inhibit release of neurotransmitters (2)
Botulinum toxin, tetanus toxin
Same activity inside cell, but different target cell causes different manifestations of toxin
- Zinc dependent endopeptidases
- inactivate SNARE proteins required for exocytosis
Botulinum toxin
anaerobic → can be ingested with home canning
Flaccid paralysis (inhibits release of ACh at myoneuroal junctions)
Tetanus toxin
anaerobic → requires deep wound that is anaerobic
Rigid paralysis inhibits (inhibit NT release from inhibitory interneurons in spinal column)
Bacterial protein toxins
aka ?
3 characteristics
aka EXOtoxins
Heat-labile, immunogenic, neutralized by abs
Lipopolysaccharides (LPS)
aka ?
ENDO toxin
Part of outer cell membrane of gram-negative organisms
Can also be released and bleb off into the bloodstream
PAMP recognized by innate immune system, elicits host response
Low dose of LPS → activates macrophages, B cells, complement
High dose of LPS → DIC
Toxins with intracellular targets
must cross plasma membrane
Bi-functional proteins: separate domains designated A (active) and B (binding)
Susceptibility or resistance to toxins determined by presence/absence of receptors on target cell
Use normal membrane constituents as receptors
Enter target cells by endocytosis
Active portion of toxin translocated to cytosol to interact with target
Toxoid
immunogenic but NOT toxic
Used as vaccines for protection against toxin-mediated diseases
Passive immunization
abs given to patient for temporary protection against toxin or infectious agent - neutralize specific toxin extracellularly (before toxin enters the cell)
Limited duration of immunity (abs degraded)
Active immunization
give toxoid to elicit production of specific anti-toxic abs
Primary series + periodic booster doses to maintain protection
Active immunity persists for many years due to immunologic memory
Immunotoxins
hybrid molecules, toxin fragment (without receptor binding domain) linked to ligand, ab or hormone that binds specific receptor (different receptor from native toxin)
Enable immunotoxin or hormonotoxin to bind cells that express the alternative receptor and intoxicate them
Designed to kill tumor cells with tumor-specific receptor, but not kill normal cells without receptor
Antitoxins
bind to toxins and prevent their toxicity (neutralization)
DO NOT prevent infection by toxin producing bacteria, or reverse effects after toxin has entered host cells
Streptococcus pyogenes is also known as ________.
It is Gram _____ _______
Group A strep (B-hemolytic)
Gram + cocci
Types of infections seen with strep pyogenes infection (5)
1) Glomerulonephritis (due to cross reactive ab)
2) Rheumatic fever (cross-reactive ab)
3) Infective endocarditis
4) Skin/wound infections (cellulitis)
5) Strep throat
Infective endocarditis associated with strep pyogenes differs from rheumatic fever in that…
bacterial infection of the heart valves themselves - not due to cross-reactive ab
M protein
2 main functions
primary virulence factor of strep pyogenes
-surface exposed protein
→ inhibits phagocytosis / killing by PMNs
→ enhances adherence to epithelial cells
Why are there repeated infections associated with strep pyogenes? What is associated with recovery?
> 70 serotypes based on antigenic dif. in M protein → repeated infection
-M protein specific ab makes bacterial cell susceptible to killing, associated with recovery and immunity (to all antigenically related strains)
Strep pyogenes is a normal flora bacteria present where?
the pharynx
How is strep pyogenes spread?
- Nasal secretions
- Droplets produced by coughing
Streptococcus pneumoniae is a gram ______ ______
aka __________
gram + cocci
pneumococcus
Types of infections associated with strep pneumoniae (invasive vs. non-invasive)
Noninvasive:
- Pneumonia (~60% of bacterial pneumonia)
- Sinusitis
- Otitis media
- Bronchitis
Invasive:
- Meningitis
- Bacteremia
Strep pneumoniae has a __________ which allows it to grow and evade host defenses. Ab to this is associated with…
antiphagocytic polysaccharide capsule
(>91 different serotypes)
Recovery/immunity due to anti-capsular ab
Why are the very young more susceptible to strep pneumoniae infection?
Very young more susceptible because less able to make ab to polysac capsule
-must give vaccine with conjugate polysaccharide
Strep pneumoniae is a bacteria that is part of our normal flora where?
Upper respiratory tract
People most susceptible to strep pneumoniae?
very young or old
alcoholism (mucocillary defect)
respiratory viral infection
Enterococcus faecalis is a gram ______ _______
gram + cocci
Enterococcus facecalis abx resistance
Intrinsic and emerging acquired abx resistance (Vancomycin-R)
Common infection sites of enterococcus faecalis (3)
1) *Urinary tract (travels from GI → across perineum → up urethra = infection)
2) Surgical wounds
3) Biliary tract
Transmission of enterococcus faecalis
Pt to pt on hands of healthcare workers or medical devices
Enterococcus faecalis is a normal flora present in __________, and thus frequently casues _________
GI tract
Frequently cause of nosocomial infections
Clostridium difficile is a gram _____ _____.
gram + rod
Two MOST important characteristics of Clostrium bacteria
STRICT ANAEROBES
endospore formers
Clostridium difficile abx resistance
Resistant to most abx
-spores resistant to hand sanitizer
Manifestation of clostridium difficile infection
Diarrhea/pseudomembranous colitis following abx tx for unrelated conditions (esp. Clindamycin)
**disease due to depletion of intestinal flora = C. difficle overgrowth
Virulence factor of Clostridium difficile
Two discrete toxins that damage intestinal mucosa = responsible for observed pathology and symptoms [enterotoxin + cytotoxin]
Clostridium difficile is a normal flora present in the _______. It is thus responsible for many __________
GI tract
Nosocomial hospital acquired infection
-Usually from pt’s own gut flora
C. Diff is associated with __________ in the hospital and is treated with ________
antibiotic associated diarrhea
TX: stop abx use, vancomycin or **metronidazole
Clostridium tetani
- Spores present in soil and animals
- Local infection must be anaerobic → toxic production
Manifestation of clostridium tetani and mechanism of action
Retrograde transport of toxin to CNS
Block INHIBITORY INTERNEURONS in CNS
Prevents you from relaxing musculature
→ Spastic paralysis
Vaccine and antitoxin for tetanus
Vaccine for tetanus (inactivated toxin)
Natural immunity does NOT occur - dose for immunization is more than dose that will kill you
Antitoxin - can be given after tetanus exposure
Clostridium botulinum
Spores in soil and animals, can contaminate canned food
Botulinum is heat resistant (not killed with canning)
Manifestation of clostridium botulinum and mechanism of action
Toxin blocks ACh transmission at neuromuscular junction→ flaccid paralysis, respiratory failure
Unable to innervate the musculature
Staph aureus vs. clostridium perfringens food poisoning
Staph - from super-antigen contaminated food (pre-made toxin ingested) –> fast onset food poisoning
Clostridium perfringens - ingest microbe which then produces toxin (toxin made in vivo) –> slow onset food poisoning
Clostridium perfringens manifestations of infection (2)
1) wound infections
2) food poisoning
strict anaerobe, makes spores
Alpha toxin
phospholipase that kills phagocytic cells and muscle tissue
- produced by Clostridium perfringens
- responsible for wound infections
Mechanism of action of food poisoning associated with Clostridium perfringens
Enterotoxin - exotoxin that acts on the gut
Ingest organisms from contaminated food
Toxin produced in vivo
Site of action is small intestine
Mycoplasma Pneumoniae is special because…
it has no cell wall!
–> NOT susceptible to penicillins, vancomycin
Type of infection associated with Mycoplasma Pneumoniae
Atypical pneumonia:
- More common in younger persons (5-20 yrs)
- Easily transmitted from person-person by respiratory secretions
- Occurs in any season
- Long period of shedding and very low infectious dose
- Mild disease (“walking pneumonia”)
- Non-productive cough
Mechanism of action of Mycoplasma pneumoniae
Adheres to respiratory epithelial cells
Bacterial growth is extracellular
Produces H2O2 and superoxide radicals → damage host tissue
Escherichia coli is a gram ______ ______
gram - rod
E. Coli abx resistance?
Common resistance via acquisition of drug-resistant plasmid
E. Coli is normal flora where?
the large intestine
Types of infections associated with E. Coli (3)
GI disease
UTI
Abdominal infections
-Many different strains with varying pathogenic potential
Mechanism of GI infection of E. coli (2 essential properties)
- Adherence to intestinal mucosa (pili)
2. Toxins that disrupt the electrolyte balance in the gut (GI disease)
Mechanism of UTI infection of E. coli (3)
- Adherence to bladder epithelium
- Specific interactions with bladder epithelial cells
- Hemolytic = which are uncommon in the bulk of the intestinal population
How do you acquire an E. coli GI infection?
drinking contaminated water or eating contaminated food
How do you acquire an E. coli UTI infection?
endogenous flora from GI tract gets into urethra → bladder → kidney = access to UT
-special strains getting into the wrong place
How do you acquire an E. coli infection in the abdomen?
Release/escape contents of colon to peritoneal cavity and adjacent tissues
-typically mixed infections with anaerobic bacteria –> anaerobic abdominal abscess
ETEC (Enterotoxigenic E. Coli)
- self-limiting
- may require fluid replacement
- GI infection
Psuedomonas aeruginosa is a gram _____ _____
gram - rod
Psuedomonas aeruginosa abx resistance?
Intrinsic resistance of P. aeruginosa to many abx
-difficulties delivering drug to site of bacterial replication
Typical infections associated with pseudomonas aeruginosa (3)
- Infection of traumatic injuries, surgical wounds, and especially BURNS
- Chronic lung infection of CF pts.
- Hospital acquired infections (UTI, pneumonia)
Psuedomonas aeruginosa is a common bacteria where?
the environment
-most people are highly resistant to infection by PA
P. aeruginosa and CF
- CF pts make copious, viscous bronchial secretions → stasis in lungs, predisposes pt to infection.
- Early in life, pulmonary infections with S. aureus are relatively common, but are usually control with antimicrobials.
- CF pts become chronically infected with P. aeruginosa by 15-20
- aided by intrinsic resistance to many anti-staph drugs
- Chronic lung infection with P. aeruginosa often cause of death in CF pts.
P. aeruginosa bacteria are bad in CF patients because they are protected from phagocytes in the lungs by… (3)
This all leads to…
1) viscous lung secretions
2) mucoid exopolysaccharide made by bacteria
3) bacterial toxins
→ progressive damage to lungs due to toxins and host immune response
Neisseria gonorrhoeae is a gram _____ ______
gram - diplococci
Neisseria gonorrhoeae acquires antigenic variation via what?
Antigenic variation – change in pilus
-randomly modifies a.a. sequence of pilus protein = dramatic change in antigenic site
Common infections associated with Neisseria gonorrhoeae (5)
1) Gonorrhea
2) Conjuctivits: leads to blindness in infants born to infected mothers (TX with abx at time of birth to prevent)
3) Urethritis
4) Fibrosis
5) Infertility
Neisseria gonorrhoeae uses a _______ for ___________ and _______ as a key requirement for its virulence
pilus
adherence, and to avoid killing by neutrophils
-ab against pilus protective for that strain
Neisseria gonorrhoeae in males vs. females
Males = asymp. to urethritis
Female = infection of cervix and urethra, ascending infection including uterine tubes = fibrosis and infertility
Bacteroides fragilis is a gram _______ _______ that is ________
gram - anaerobic rod
aerotolerant
Typical infections associated with bacteroides fragilis
anaerobic abscess below the diaphragm
3 virulence factors of bacteroides fragilis
1) Tissue-destructive enzymes
2) Capsule (protects from phagocytosis)
3) Superoxide dismutase (protects an organism from the lethal effects of oxygen)
Bacteroides fragilis is a normal flora where?
colon (in small numbers only)
Chlamydia trachomatis is a ____________
obligate intracellular bacterium
Infections associated with Chlamydia trachomatis (3)
Trachoma → chronic infection of conjunctiva → blindness
Genital infections (STD)
Neonatal infections → conjuctivitis and pneumonia
Chalmydia trachomatis grows __________ and infects via ________
grows in vacule within host cell and infects via elementary bodies
Chalmydia trachomatis infection in males vs. females
- Males → urethritis
- Females → urethritis, cervicitis, PID
associated with gonorrhea infections
